Fibroin and sericin from Bombyx mori silk stimulate cell migration through upregulation and phosphorylation of c-Jun.
Fibroin and sericin from Bombyx mori silk stimulate cell migration through upregulation and phosphorylation of c-Jun.
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DOI：
10.1371/journal.pone.0042271
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Nicolás FJ
中科院分区：
文献类型：
--
作者：
Martínez-Mora C;Mrowiec A;García-Vizcaíno EM;Alcaraz A;Cenis JL;Nicolás FJ
伤口愈合是一个生物学过程，旨在恢复遭受损伤的组织。伤口愈合的一个重要阶段是产生能够完全替代伤口表皮的基底上皮。从桑蚕丝的丝心蛋白和丝胶蛋白中提取的各种产品用于刺激伤口愈合。然而，到目前为止，这种现象背后的分子机制尚未阐明。这项工作的目的是使用细胞模型确定丝蛋白的伤口愈合特性的分子基础。为此，我们在使用MDA-MB-231和Mv 1 Lu细胞的伤口愈合划痕试验中测定丝心蛋白和丝胶蛋白。这两种蛋白质刺激细胞迁移。此外，用丝胶蛋白和丝心蛋白处理涉及伤口愈合过程的关键因素，例如上调c-Jun和c-Jun蛋白磷酸化。此外，丝素蛋白和丝胶蛋白刺激ERK 1/2和JNK 1/2激酶的磷酸化。所有这些实验都是在上述一些细胞信号传导途径的特异性抑制剂存在下进行的。结果表明，MEK、JNK和PI 3 K通路参与了丝素蛋白和丝胶蛋白刺激的细胞迁移。这三种激酶的抑制防止c-Jun上调和丝素蛋白或丝胶蛋白的磷酸化。在人角质形成细胞系HaCaT中测试丝素蛋白和丝胶蛋白，结果相似。总之，我们的研究结果表明，丝心蛋白和丝胶蛋白通过激活MEK、JNK和PI 3 K信号通路启动细胞迁移，最终激活c-Jun。
Wound healing is a biological process directed to the restoration of tissue that has suffered an injury. An important phase of wound healing is the generation of a basal epithelium able to wholly replace the epidermis of the wound. A broad range of products derived from fibroin and sericin from Bombyx mori silk are used to stimulate wound healing. However, so far the molecular mechanism underlying this phenomenon has not been elucidated. The aim of this work was to determine the molecular basis underlying wound healing properties of silk proteins using a cell model. For this purpose, we assayed fibroin and sericin in a wound healing scratch assay using MDA-MB-231 and Mv1Lu cells. Both proteins stimulated cell migration. Furthermore, treatment with sericin and fibroin involved key factors of the wound healing process such as upregulation of c-Jun and c-Jun protein phosphorylation. Moreover, fibroin and sericin stimulated the phosphorylation of ERK 1/2 and JNK 1/2 kinases. All these experiments were done in the presence of specific inhibitors for some of the cell signalling pathways referred above. The obtained results revealed that MEK, JNK and PI3K pathways are involved in fibroin and sericin stimulated cells migration. Inhibition of these three kinases prevented c-Jun upregulation and phosphorylation by fibroin or sericin. Fibroin and sericin were tested in the human keratinocyte cell line, HaCaT, with similar results. Altogether, our results showed that fibroin and sericin initiate cell migration by activating the MEK, JNK and PI3K signalling pathways ending in c-Jun activation.
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影响因子：
4.8
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